Electroacupuncture Ameliorates Neuroinflammatory Injury in CPSP Rats by Inhibiting the LncRNA MEG3-Mediated...

Area of Science:

• Neuroscience
• Pain Management
• Inflammation Research

Background:

• Central poststroke pain (CPSP) is a debilitating condition with limited treatment options.
• The precise mechanisms underlying EA's therapeutic effects on CPSP remain incompletely understood.
• Neuroinflammation is implicated in the pathophysiology of CPSP.

Purpose of the Study:

• To investigate the role of EA in modulating central nervous system inflammation in a rat model of CPSP.
• To explore the involvement of long non-coding RNA MEG3 and the Wnt/β-catenin pathway in EA's analgesic effects.

Main Methods:

• A CPSP rat model was induced via collagenase IV injection into the thalamus (VPL).
• Rats received electroacupuncture (EA) treatment; MEG3 was manipulated using adeno-associated virus vectors.
• Pain thresholds, neuronal injury, and inflammatory markers (GFAP, Substance P, TNF-α, IL-1β, IL-6) were assessed.
• Gene and protein expression of MEG3, Wnt3a, and β-catenin were analyzed via qRT-PCR and Western blotting.

Main Results:

• EA treatment significantly inhibited MEG3 expression and neuroinflammatory injury in the VPL region of CPSP rats, reducing hyperalgesia.
• Overexpression of MEG3 counteracted EA's inhibitory effects on the Wnt/β-catenin pathway, worsening pain and neuroinflammation.
• Suppression of MEG3 alone mimicked the therapeutic effects of EA, indicating its crucial role.

Conclusions:

• EA alleviates neuroinflammation and pain in CPSP rats by suppressing MEG3 expression.
• EA exerts its therapeutic effects, in part, by regulating the Wnt/β-catenin signaling pathway through modulation of MEG3.